Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS

Objective

Aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder (AQP4+ NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and multiple sclerosis (MS) are pathophysiologically distinct neuroinflammatory disorders. Complement activation is a major mechanism of injury in AQP4+ NMOSD, whereas its role in MS is complex and in MOGAD controversial. We aimed to compare complement components and cytokines between AQP4+ NMOSD, MOGAD, and MS.